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Corticosteroid glaucoma.

J François, V Victoria-Troncoso

    Ophthalmologica. Journal International D'Ophtalmologie. International Journal of Ophthalmology. Zeitschrift Fur Augenheilkunde
    |January 1, 1977
    PubMed
    Summary
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    Corticosteroids can worsen eye fluid drainage by preventing enzymes from breaking down eye tissues. The cortisone test indicates whether eye cells are sensitive to this effect, impacting glaucoma risk.

    Area of Science:

    • Ophthalmology
    • Cell Biology
    • Biochemistry

    Background:

    • Non-depolymerised mucopolysaccharides in the anterior chamber angle can lead to ocular edema.
    • This edema obstructs the trabeculae, potentially increasing intraocular pressure.
    • Lysosomal enzymes physiologically depolymerise mucopolysaccharides, preventing obstruction.

    Purpose of the Study:

    • To investigate the role of corticosteroids in the anterior chamber angle.
    • To understand the mechanism by which corticosteroids impede the natural prevention of trabecular obstruction.
    • To explore the basis for variable responses to corticosteroid treatment in the eye.

    Main Methods:

    • Analysis of mucopolysaccharide hydration and depolymerisation in the anterior chamber angle.

    Related Experiment Videos

  • Investigation of lysosomal enzyme activity and its regulation by corticosteroids.
  • Assessment of goniocyte sensitivity to corticosteroids and correlation with the cortisone test.

    • Main Results:

    • Corticosteroids reinforce lysosomal membranes, inhibiting the release of catabolic enzymes.
    • This inhibition facilitates trabecular obstruction by preventing mucopolysaccharide depolymerisation.
    • Goniocytes exhibit varying degrees of corticosensitivity, influencing the cortisone test outcome.

    Conclusions:

    • Corticosteroids can exacerbate ocular edema and trabecular obstruction by interfering with natural enzymatic processes.
    • The cortisone test's positivity or negativity is determined by the predominance of corticosensitive or corticoresistant goniocyte clones.
    • This highlights a cellular basis for differential responses to corticosteroid therapy in ocular conditions.